Associated Papers
Fusion oncoproteins and cooperating mutations define disease phenotypes in NUP98-rearranged leukemia.
Umeda M et al.
Blood, 2025
40700635 (PubMed )
Supplement: BLOOD_BLD-2025-028993-mmc2.xlsx › Supplementary_Table_6
Clinically relevant variants detected in Chinese children with global developmental delay/intellectual disability: An exome-wide sequencing study.
Qiao Y et al.
Genes & Diseases, 2025
40212794 (PubMed )
Supplement: mmc2.xlsx › Sheet1
Fusion oncoproteins and cooperating mutations define disease phenotypes in NUP98-rearranged leukemia.
Umeda M et al.
Medrxiv : the Preprint Server for Health Sciences, 2025
39974131 (PubMed )
Supplement: media-2.xlsx › Supplementary_Table_6
A new genomic framework to categorize pediatric acute myeloid leukemia.
Umeda M et al.
Nature Genetics, 2024
38212634 (PubMed )
Supplement: 41588_2023_1640_MOESM5_ESM.xlsx › Extended_data_Fig.1_source_data
Integrative Genomic Analysis of Pediatric Myeloid-Related Acute Leukemias Identifies Novel Subtypes and Prognostic Indicators.
Fornerod M et al.
Blood Cancer Discovery, 2021
34778799 (PubMed )
Supplement: bloodcandisc-2-586-s001.xlsx › Supplementary_Table_12
[A case with MPPH3 syndrome caused by a novel variation in CCND2 gene].
Li LF et al.
Zhonghua Er Ke Za Zhi = Chinese Journal of Pediatrics, 2021
Clinical impact of the subclonal architecture and mutational complexity in chronic lymphocytic leukemia.
Nadeu F et al.
Leukemia, 2018
28924241 (PubMed )
Supplement: leu2017291x1.pdf
Mutations in the CCND1 and CCND2 genes are frequent events in adult patients with t(8;21)(q22;q22) acute myeloid leukemia.
Eisfeld AK et al.
Leukemia, 2017
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